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Archive for May, 2010

Heart is one of the unique organs , that a physician can touch and feel before diagnosing a disease .The fact that ,  the heart is located superficially within the thoracic cavity makes tactile examination possible . The current generation cardiologists should realise cardiac palpation was a huge scientific specialty by itself centuries ago . Apical impulse demonstration  in class rooms  would go on for hours together in the days of Leannc and Dressler .

It is an irony , when we are able to see and feel many areas of the heart in the direct vision ( RV parasternal impulse, pulmonary arterial pulsation, contractility of LV ) we got addicted to imaging modalities now.

This article tries to extrapolate the  morphology of  apical impulse  with that of ehocardiographic LV function . A normal apical impulse is a very subtle impulse often absent in a third of population.Some times it is called tapping impulse .The  two common abnormalities  of apical  impulse are hyperdynamic and heaving .

Read the link for normal apical impulse

A hyperdynamic apical impulse

The  hyperdynamic apical impulse is diffuse (Occupying at least two rib spaces >  3Sqcms) and very active  with brisk motions visible to naked eye .This implies the leftventricle is dilated significantly and the wall is not much hypertrophied. This is eccentric LV enlargement . It also tells us the LV function is well-preserved as the term hyperdynamic infers very active LV .It is obvious , a dysfunctional LV can not be hyperactive. A hyperdynamic LV apex in a patients with AR or MR indicates they will do well after surgery for the simple reason their LV function is preserved. In the same logic a patient with hyperdynamic apex often complaints of palpitation as the apex hits the chestwall . Which is a good sign with reference to LV function .

Note :A patient with heaving apex rarely complaints of palpitation.

Hyperdynamism occur in systole or diastole ?

Logic would say apical impulse would be palpable only in  systole .But in a hyperdynamic LV diastolic phase is also palpable (A palpable S3 is common associate of hyperdynamic apex)

Heaving apical impulse

The term heaving apex by definition indicate there is a brief localized sustained LV apex lasting at least 50% of systole.

  •  Aortic stenosis with normal LV function
  • Any dysfunctional and dilated LV which increases the after load

The sustained lift may disappear with very severe LV dysfunction , apical impulse is barely perceptible in failing hearts . A sustained LV apex suggest reduced dp/dt of  LV contractility .

Relationship between apical impulse character and LVH ?

Hyperdynamic LV apex is rare to be associated with LVH .Except probably in HOCM where the LV systole is interrupted very early in the ejection phase.

Heaving apex can be a marker of LVH .But, the onset of LV dysfunction can confound this finding.

Can a hyperdynamic and heaving characters occur together in apical impulse?

We have been taught cardiology with a black and white learning concept but unfortunately science more often exists in shades of grey An apical impulse can indeed have characters of both . A diffuse apical impulse with a heaving nature is common in regurgitating lesions with the onset of LV dysfunction Such situation can occur in LV apical aneurysm

Final message

Looking for apical impulse in current cardiology practice  may be considered as  the most foolish job  a physician can indulge !

Ask the secretary to record the history ,  take an ECG, do an Echo  , send both deserving (and of course  many undeserving patients too !)  to cath lab at the earliest  . . . This is the  modern-day cardiology mantra !

This article , does not vouch  for the accuracy of   what  some may consider as  a  “medieval clinical sign” . But , it  confers the patient  a better rapport  strightaway   as  the physician  puts  his or her hand on the patients heart  . Some  call this  as a healing touch ! It work  wonders in many !

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Let ventricle is an elliptical or ovoid chamber .The pattern of LV enlargement can vary considerably in different pathologies. We know a dilated , globular heart is the typical feature of terminal congestive heart failure. But in the early stages of cadiac enlargement there are some distinct differences in the contour. (Aortic stenotic lesions retain the ellipitical shape till late in the course )

LV enlargement due to mitral regurgitation is somewhat different from aortic regurgitation. A globular configuration occurs more often in severe MR than AR. This is due to the fact, the long axis and short axis ratio of LV  is maintained till late in the course  of aortic valve disease . Cardiac long axis enlargement is more pronounced in aortic valve disease than in MR. The AR jet reaches LV  at a higher pressure gradient (Diastolic pressure of aorta) than mitral inflow velocity . (Often mimic physiological flow with an S3)

For a given degree of regurgitant volume AR will cause more cardiac enlargement than MR. In the same note , one should realise  the LA becomes huge in MR which receives high pressure regurgitant jet . Further ,mitral valve disease is more likely to result in early PAH and that results in right sided chamber enlargement giving the cardiac contour a more globular configuration

Is the cardiac contour different in rheumatic and degenerative(Myxamatous) mitral regurgitation ?

Yes , rheumatic MR results in less enlargement of the base of the heart as the fibrotic process restricts and restrains LV and prevents uncontrolled LV dilatation . In fact , giant LV are often  reported in mitral regurgitation due to mitral valve prolapse than rheumatic MR.

Why the configuration of LV important in the management of cadiac failure ?

The globular configuration of LV implies , the papillary muscles are attached in a disadvantaged angle and keep the free wall stress high. Specialized procedures are required to restore the LV shape especially in secondary to mitral annular dilatation. Isolated aortic valve disease rarely require LV remodeling surgeries , even if AVR is done late stages.

What is the maximum dimension of LV reported in cardiac failure ?

The upper limit of normal for LV diastolic dimension is 5.6cms. In MR it often reaches 6-7 cms . The maximum of 10cm has been reported with AR. An LV beyond this level looses it’s elasticity and likely to be incompatible with survival unless LV reduction surgeries like Batista are performed.

Is secondary valvular cardiomyopathy an accepted entity ?

 The  term cardiomyopathy when originally defined decades ago ,  required exclusion of all known cases of cardiac enlargement. But now we have a more liberal working concept , if the LV enlarges disproportionate to the loading conditions of the valvular lesions  , secondary cardiomyopathy is said to be present. If cadiomyopathy sets in,  the cardiac shape invariably takes in a globular configuration irrespective of the valvular lesions. So, the simple parameter of shape of LV in X ray chest can give us a clue regarding the outcome in valvular heart disease.

Further reading

Also read sphericity index by echocardiography A spherical LV can be easily quantified by echocardiography

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 Excercise physiology has been studied most extensively in the last century.The hemodynamic impact of excercise in various disorders of heart has been well established.
Dyspnea on exertion is the commonest symptom in clinical cardiology practice. It is well-known pulmonary stretch receptors located in pulmonary vasculature is one of the  major mechanism of dyspnea.

Excercise increases the cardiac output manyfold.Transporting  up to 10-12 litres of blood every minute across the lungs with a narrow pressure  head (about 10 mmhg ) is not an easy job . It needs lot of lung discipline .

It is surprising to note, there is little data on excercise induced pulmonary hypertension in the evaluation of patients with unexplained dyspnea.

We know, excercise increases the systemic blood pressure ,we  presume it should not raise the PAP (however severe the exertion is 1 )as pulmonary circulation  is a  high compliant low pressure system. 

Is our presumption correct ?

Exercise induced PAH can occur in both   health and disease 

In patients with preexisting disease

  • Stress induced LV dysfunction and resultant raise in LVEDP-PCWP-PAP .This is the most common mechanism in valvular and myocardial  disease.

Apparently healthy population

  • Excercise  induced PAH as a  marker for silent CAD .
  • Transient Hyperkinetic PAH* (Note :Here PCWP is usually normal )

This is similar  to hypertensive response to EST in systemic circulation.Existence  of this entity , is controversial, But this may reflect  reduced pulmonary vascular reserve  or reduced pulmonary nitric oxide secretion.

*The main difference here is the PAH is more often an  isolated systolic PAH. While LV dysfunction induced PAH is  a combined diastolic and systolic PAH .
How to assess excercise induced  PAH ?
It is not an easy job. Invasive catheter derived pressure measurements have been done ,but it is not practical .

The simplest way is to look for the TR /PR jet in echo in both pre and post excercise phase.

Final message

Excercise induced PAH is an inadequately studied entity in cardiology , in spite  it’s great significance .
This phenomenon is observed  in both diseased and normal heart.

The quantum of excercise induced PAH  is  widely variable depending upon the cardiac  status especially  LV function and the  functional integrity of pulmonary microvasculature .

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Ventricular septal defect(VSD) is one the commonest congenital heart disease . Right from the days of Gasul , Abbot, and Keith we have analysed the natural history for nearly a century . VSD is an intriguing congenital heart disease where a child can develop a florid cardiac failure within weeks of birth in one end to a totally asymptomatic adult with a benign cardiac acoustics defect (Namely a systolic murmur in the left parasternal area.) But for this murmur , the patient would be labeled absolutely healthy.

 In between these two spectra is the huge population of VSD that gets closed spontaneously. A rough estimate says 60 % of all small VSDs get closed by age 10 .

So ,what we are supposed to do once a child is diagnosed of VSD ?

Should we close or should we wait ?

The indication for closing a VSD is discussed elsewhere ( Read this link )

 What are the factors that determine VSD closure ?

  • The size
  • The site
  • Age of the child
  • The Rim morphology
  • Associated lesions*
  • Hemodynamic stress
  • Inherent tissue factors
  • Infection **

* Associated defects like PDA, RVOT obstruction are strong deerrants against spontaneous closure

General rules of VSD closure

 Size

VSDs <5mm have great chance of closing Large VSD > 1cm is rarely get closed .

Supracristal VSDs located sub arterially are immune to spontaneous closure however small the size is .

Location & Site

 VSDs that are located exclusively within the membranous septum rarely close . VSDs which are located in the perimembranous area (With at least 50% circumference is fenced by muscular or trabecular septum has the greatest potential to close by natural forces.)

Isolated muscular VSD if large can not get closed . Inlet VSD has anatomical difficulty to get closed.

Rim Morphology

 Small muscular VSDs have a potential to close , but it is believed differential cellular lining of VSD rims (Eg : A combination of muscle, membrane , is more likely to close .)

 Process of tissue growth As the child grows the it is expected the heart will outgrow the lesion . This is thought to be the commonest mode of VSD closure. As the IVS mass increases as he child grows it brings he rims together . But logic would suggest unless some degree of neocardiac proliferation occur a VSD may never get closed completely .

Some times even large VSDs try to close with the help of the neighboring structures like septal tricuspid valve leaflet . Indeed this can be the dominate mode of closure in many. This can induce a tricuspid regurgitation .

**Role of infection

Paradoxically an episode of infective endocaditis in the edges of VSD accelerate the process of approximation of tissue plane and healing .

 Relation with Pulmonary arterial hypertension (PAH)

 Once PAH sets in the VSD never gets closed spontaneously , This may be due to all VSDs that result in PAH has to be significantly large

 Can a VSD get larger progressively?

In physics and hydraulics a hole under hemodynamic stress is destined to progress In human biology this is thought to be rare .Post MI VSRs can behave in an unpredictable manner as he edges of the defect a often softened and prone for tissue plane dissection and extension .

Why some VSDs never close ?

It is clear , size and location matters the most , but there are other issues some of them may be unique tissue properties .

Why is it important to know the biology of VSD closure ?

In this era of interventional cardiology we are using mechanical devices to close VSDs and ASDs .It is fraught with many technical issues. If there is a biological glue or membrane that can be delivered by catheter to close small VSDs or ASDs .

 So for no therapeutic approach to hasten the natural closure of these defects has been practiced .Further research is required to explore the cellular adhesiveness and help accelerate closure of these defects.

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Chronic total occlusion is the cardiologist’s  daymare .Here is an article that adds on to 1ooth technique to cross the chronic total occlusion within the coronary artery !

If only we succeed in  this  Arabin magic , in the cath lab we can open the doors of  all CTOs .

This technique is based on the principle  to push the hard plaque  into the adjacent side branch like a sliding door,   if the pateint has one !

The only isssue  with this  technique  could be the    “cave door”  may close again immediately  as it did for Alibaba    !

Reference

 http://www.ncbi.nlm.nih.gov/pubmed/20088015

http://www3.interscience.wiley.com/journal/122619470/abstract

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